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Vitamin D

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Vitamin D is a hormone precursor that contributes to the maintenance of normal levels of calcium and phosphorus in the blood. Despite its name, vitamin D is not a true vitamin, but it could best be described as a conditional vitamin, since human skin can create it in some circumstances. Vitamin D is also known as calciferol.

Overview

Vitamin D plays an important role in the maintenance of an intact and strong skeleton. Its primary task is to regulate the amount of calcium and phosphorus in the blood by ensuring correct intake and secretion (from intestines and urine, respectively).

Several studies show that vitamin D also regulates the growth of skin cells. Psoriasis gives shell-like skin as a result of uncontrolled cell growth. A vitamin D compound is used in the treatment of this disease.

The human body produces its own vitamin D in the skin. This process is dependent on ultraviolet radiation from sunlight. However, Vitamin D should not be excluded from the diet – this is especially important for people who do not receive sufficient sunlight.

Forms of Vitamin D

Vitamin D3, also known as cholecalciferol, is a form of vitamin D that is made by the human body. It is made in the skin when 7-dehydrocholesterol reacts with UVB ultraviolet light with wavelengths 290 to 315 nm. This can be found in sunlight when the sun is high enough above the horizon for UVB to penetrate the atmosphere and is responsible for the production of cholecalciferol. Up to 20,000 IU can be made in the skin only after one minimal erythemal dose of exposure, or until the skin just begins to turn pink.

Vitamin D2 is derived by irradiating fungi to produce ergocalciferol. Ergocalciferol does not naturally occur in the human body unless it is added by supplementation. In the rat, D2 is more effective as a vitamin than D3, and in the squirrel monkey and the chick, D3 is more effective[1]. In humans, D3 is more effective than D2 at increasing 25-hydroxyvitamin D, the circulating reservoir of the vitamin D hormone. In certain parts of the world, particularly at higher latitudes, total vitamin D input is usually not sufficient, especially in the winter, thus the recent concern about widespread vitamin D deficiency. To help prevent this, foods such as milk may be fortified with vitamin D2 or vitamin D3, typically giving 100 IU per glass. Cholecalciferol is transported to the liver where it is hydroxylated to calcidiol or 25-hydroxy-vitamin D, the form of the vitamin that the body stores. A blood calcidiol level is the only way to determine vitamin D deficiency; levels should be between 40 and 60 ng/mL (100 to 150 nMol/L) for optimal health. The most active form of the vitamin is calcitriol (1,25 dihydroxy vitamin D3), a potent hormone. Calcitriol is synthesized from calcidiol in the kidneys to perform its endocrine function of maintaining the calcium economy. Calcitriol binds to a transcription factor which then regulates gene expression of transport proteins like TRPV6 and calbindin that are involved in calcium absorption in the intestine. The general result is the maintenance of calcium and phosphorus levels in the bone and blood with the assistance of parathyroid hormone and calcitonin. A number of tissues throughout the human body also have the ability to make and regulate their own calcitriol. It is these autocrine and paracrine functions of the vitamin D system that may explain its association with a host of chronic diseases.

Vitamin D food sources

Fortified foods are the major dietary sources of vitamin D. Prior to the fortification of milk products with vitamin D in the 1930s, rickets, commonly caused by vitamin D deficiency, was a major public health problem. In the United States milk is fortified with 10 micrograms (400 IU) of vitamin D per quart, and rickets is now uncommon there.

One cup of vitamin D fortified milk supplies about one-fourth of the official estimated adequate intake of vitamin for adults older than age 50 years. Although milk is often fortified with vitamin D, dairy products made from milk (cheese, yogurt, ice cream, etc.) are generally not. Only a few foods naturally contain significant amounts of vitamin D, including:[2]

  • Fish liver oils, such as cod liver oil, 1 Tbs. (15 ml), 1,360 IU (340% Daily value)
  • Fatty fish, such as:
    • Salmon, cooked, 3.5 oz, 360 IU (90% DV)
    • Mackerel, cooked, 3.5 oz, 345 IU (90% DV)
    • Sardines, canned in oil, drained, 1.75 oz, 250 IU (70% DV)
    • Tuna, canned in oil, 3 oz, 200 IU (50% DV)
    • Eel, cooked, 3.5 oz, 200 IU
  • One whole egg, 20 IU (6% DV)

Vitamin D is commonly measured in micrograms (mcg). However, International Units (IU) is the unit of measurement for vitamin D that appears on food labels.

Nutrition

The U.S. Dietary Reference Intake (DRI) for an Adequate Intake (AI) for a 25-year old male for Vitamin D is 5 micrograms/day (200 units/day). This rises to 15 micrograms/day (600 units/day) at 70.[3]

Diseases caused by deficiency

Vitamin D deficiency is known to cause several bone diseases, due to insufficient calcium or phosphate in the bones:

  • Rickets: a childhood disease characterized by failure of growth and deformity of long bones.
  • Osteoporosis: a condition characterized by fragile bones.
  • Osteomalacia: a bone-thinning disorder in adults that is characterised by proximal muscle weakness and bone fragility. Osteomalacia can only occur in a mature skeleton.

Pioneering work in isolating vitamin D and determining its role in rickets was done by Edward Mellanby in 1918-1920. Vitamin D deficiency is endemic in dark skinned races living in high latitudes (see below).

Vitamin D malnutrition may possibly be linked to chronic diseases such as cancer (breast, ovarian, colon, prostate, lung and skin and probably a dozen more types), chronic pain, weakness, chronic fatigue, autoimmune diseases like multiple sclerosis and Type 1 diabetes, high blood pressure, mental illnesses (depression, seasonal affective disorder and possibly schizophrenia) heart disease, rheumatoid arthritis, psoriasis, tuberculosis, periodontal disease and inflammatory bowel disease.[4]

Who may need extra vitamin D to prevent a deficiency

Older people (age 50 and over) have a higher risk of developing vitamin D deficiency. The ability of skin to convert 7-dehydrocholesterol to pre-vitamin D3 is decreased in older people. The kidneys, which help convert calcidiol to its active form, sometimes do not work as well when people age. Therefore, many older people may need vitamin D supplementation.

Newborn infants who are exclusively breastfed may require vitamin D supplements. Breast milk does not contain significant levels of the vitamin, and although infants could receive this vitamin from sunlight, it is usually not recommended that small infants be exposed to sunlight in the levels required to produce a sufficient amount of vitamin D. Infant formula is generally fortified with vitamin D, so this requirement only applies to breastfed infants.

Dark-skinned people living at higher latitudes may require extra Vitamin D because their high level of skin pigmentation generally retards the absorption of UV rays. This does not pose a problem in tropical areas, where the amount of sunshine is so high that enough Vitamin D is produced despite the dark skin color. At higher latitudes, however, the decreased angle of the sun's rays, reduced daylight hours in winter, and protective clothing worn to guard against cold weather prove detrimental to the absorption of sunlight and the production of Vitamin D. Light-skinned people at higher latitudes also face these problems, but the lower amount of pigmentation in their skin allows more sunlight to be absorbed, thereby reducing the risk of Vitamin D deficiency (conversely, light-skinned people are disadvantaged in the tropics, as they are more susceptible than dark-skinned people to intense sunlight and resultant problems such as sunburn, etc.).

There is also evidence that obese people have lower levels of the circulating form of vitamin D, probably because it is deposited in body fat compartments and is less bioavailable, so obese people whose vitamin D production and/or intake is marginal or inadequate are at higher risk of deficiency.

Those who avoid or are not exposed to summer midday sunshine may also require Vitamin D supplements. In particular, recent studies have shown Australians and New Zealanders are Vitamin D deficient[5], particularly after the successful "Slip-Slop-Slap" health campaign encouraging Australians to cover up when exposed to sunlight to prevent skin cancer. Ironically, a vitamin D deficiency may also lead to skin cancer. Still, only a few minutes of exposure (probably 6 times more in dark-skinned people) is all that is required; the production is very rapid. However, since even a few minutes of unprotected ultraviolet exposure a day increases the risk of skin cancer and causes photoaging of the skin, many dermatologists recommend supplementation of vitamin D and daily sunscreen use.

Adults taking vitamin D in vitamin pills containing 5 micrograms (200 IU) per day are not protected against vitamin D deficiency -- even though 200 IU/day is the adequate intake officially recommended up to age 50 years. Currently, the general public is advised that the safety of vitamin D intake cannot be assured beyond 50 micrograms/day (2000 IU/day). Despite a widespread recognition that current official advice to the public about vitamin D is out of date, the process for revising recommendations like the RDA has stopped, apparently for budgetary reasons. Vitamin D dietary guidelines are among the next in line for reassessment by the Food and Nutrition Board in North America.[citation needed]

Patients with chronic liver disease or intestinal malabsorption may require larger doses of vitamin D (up to 40,000 IU or 1 mg (1000 micrograms) daily). To maintain blood levels of calcium, therapeutic vitamin D doses are sometimes administered (up to 100,000 IU or 2.5 mg daily) to patients who have had their parathyroid glands removed (most commonly renal dialysis patients who have had tertiary hyperparathyroidism, but also patients with primary hyperparathyroidism) or who suffer with hypoparathyroidism. Long-term intake of these doses would be toxic in normal human beings.

Oral overdose of vitamin D3

The U.S. Dietary Reference Intake Tolerable Upper Intake Level (UL) for a 25-year old male for Vitamin D is 50 micrograms/day. This is equivalent to 2000 IU/day.

Overdose is extremely rare; in fact, mild deficiencies are far more common. While the sunshine-generated quantity is self-limiting, vitamin pills were thought not to be; and this has led to widespread concern, which may well be misplaced.

In practice, the human body has enormous storage capacity for vitamin D, and in any case all common foods and correctly-formulated vitamin pills contain far too little for overdose to ever occur in normal circumstances and normal doses.[citation needed] Indeed, Stoss therapy involves taking a dose over a thousand times the daily RDA once every few months, and even then often fails to normalise vitamin D3 levels in the body.[citation needed] However, oral overdose has been recorded due to manufacturing and industrial accidents and leads to hypercalcaemia and atherosclerosis and ultimately death. In rodents, the hypercalcaemia effect of vitamin D leads to a highly effective rat poison.[6]

The exact long-term safe dose is not entirely known, but intakes of up to 2000 IU (10x the RDA) are believed to be safe, and some researchers believe that 10,000 IU does not lead to long term overdose. It seems that there are chemical processes that destroy excess vitamin D, even when taken orally, although these processes have not been identified (in experiments blood levels of vitamin D do not continue to increase over many months at these doses as presumably would be needed for toxicity to occur.)

Note that although normal food and pill vitamin D concentration levels are too low to be toxic, cod-liver oil, if taken in multiples of the normal dose, could reach poisonous levels because of the high vitamin A content in cod-liver oil -- not the vitamin D.

Other research disputes the view that high vitamin D intake is so benign. In one study, hypercalciuria and bone loss occurred at levels of 25D above approximately 50 ng/ml.[7] Another study showed elevated risk of ischaemic heart disease when 25D was above 89 ng/ml.[8] In many chronic diseases, new research indicates vitamin D supplementation is inadvisable due to vitamin D hypersensitivity/dysregulation.

Vitamin D in cancer prevention and recovery

Recent research suggests that cancer patients who have their surgery/treatment in the summer - and therefore get more vitamin D - have a much better chance of surviving the disease than those who have their treatment in the winter when they are exposed to less sunlight. [9]

In 2005, U.S. scientists released a study, published in the American Journal of Public Health, which seems to demonstrate a beneficial corelation between Vitamin D intake and prevention of cancer. Drawing from their review of 63 old studies, the scientists claimed that taking 1,000 international units (IU) - or 25 micrograms - of the vitamin daily could lower an individual's cancer risk by 50% in colon cancer, and by 30% in breast and ovarian cancer[10]. Cancer experts, however, say that much further research is needed to provide concrete proof about Vitamin D's ability to prevent cancer.

Vitamin D Dysregulation/Hypersensitivity in Chronic Disease

There is increasing recognition that Th1 immune inflammation, occurring in rheumatic diseases can result in excessive numbers of activated macrophages converting 25-hydroxyvitamin D (25D) to its active 1,25 dihydroxyvitamin D (1,25D) hormonal form.[11][12][13][14] This can lead to vitamin D dysregulation/hypersensitivity, which can lead to hypervitaminosis D, hypercalcemia and other symptoms. This is recognized as occurring in sarcoidosis and other diseases.[15]

Serum vitamin D, measured by the precursor, 25D, may appear to be deficient in chronic diseases in which vitamin D dysregulation occurs, because it is being depleted due to excessive conversion into the active 1,25D form by macrophages.[15] In this situation, supplementation with vitamin D may lead to an even greater elevation of an already elevated level of the 1,25D hormone.[11][12]

Some of the newest research on vitamin D[12][16] emphasizes its role in combating bacteria, particular tiny L-forms, named after the Lister Institute where they were first described by Kleinberger-Nobel in 1934.[17] L-forms lack a cell wall and can hide inside cells, including immune cells, like macrophages. There is increasing evidence for this in diseases like systemic lupus erythematosus,[18] rheumatoid arthritis,[19][20][21] Crohn's disease,[22] sarcoidosis[11]Cite error: A <ref> tag is missing the closing </ref> (see the help page).[23][24] and multiple sclerosis.[12][25]

Molecular modeling research[26] indicates that 25D actually displaces 1,25D bound to the vitamin D receptor (VDR). This may block innate immunity and bacterial killing, thus suppressing the reaction associated with bacterial killing, called the Jarisch-Herxheimer Reaction. This immune suppression may explain why some studies find that vitamin D gives the appearance of being helpful in the short term. However, if bacteria are the underlying cause of the disease, this short term anti-inflammatory effect may lead to an increase in bacteria and harm occurring over several decades.[26][12][16]

Marshall showed that elevated levels of 1,25D are able to cause dysfunction of alpha 2 thyroid receptors and glucocorticoid receptors, thus interfering with endocrine function and the adaptive immune response.[27] Recently, a Fellow of the Salk Institute, Professor Ronald M. Evans, delivered a CME seminar to FDA CDER. In response to a question of what the impact on public health policy should be, given that "vitamin D" is actually a secosteroid, rather than a vitamin, he indicated that he would not supplement with "vitamin D" in the food chain.[28] However, rickets a vitamin D deficiency disease is emerging again worldwide. Many people through out the world fail to get from sunlight the vitamin D needed to prevent rickets. Fortification of dairy products such as milk is a way of staving off the disaster of rickets. [1] Whiting SJ, Calvo MS. Dietary recommendations to meet both endocrine and autocrine needs of Vitamin D.1: J Steroid Biochem Mol Biol. 2005 Oct;97(1-2):7-12. Epub 2005 Jul 25.

Success using a new antibacterial protocol (Autoimmunity Research Foundation) to treat chronic Th1 inflammatory diseases that includes lowering of vitamin D levels, supports this view of the role of vitamin D dysregulation.[12][16][11] The role of vitamin D and the vitamin D receptor (VDR) is also shown by the effectiveness of olmesartan, an angiotensin receptor blocker, as part of this new protocol. Olmesartan acts through binding to the VDR, among other effects.[11][26]

This new research on vitamin D's effects and the role of vitamin D dysregulation may require reinterpretation of much past research supporting vitamin D supplementation in the prevention and treatment of many chronic diseases.[12][16]

Human skin production of vitamin D

Vitamin D3 is produced in the skin by conversion of 7-dehydrocholesterol by UVB. Human skin exposed to sunlight can, under the right conditions, produce quantities as large as 20,000 IU in just a few minutes without any apparent toxicity. This is easily enough to avoid deficiency and builds up the body's stores.

Exposure to sunlight also destroys vitamin D, so long term exposure to sunlight cannot cause toxicity, as levels are self-adjusting.

However merely being exposed to sunlight does not automatically mean that vitamin D is produced, only the UVB in sunlight triggers vitamin D production, but UVB mainly reaches ground level when the sun is high in the sky. This occurs a few hours around solar midday (1 pm summertime). At higher latitudes, the sun is only high enough in the sky in summer. For example, in the United States, those living north of a line from San Francisco to Philadelphia (about 40 degrees of latitude) will not be able to produce it in significant quantities for 3 to 6 months a year.

Therefore from the end of summertime to the following spring humans run on stores which gradually deplete. By some estimates 10-20% of the population become at least mildly deficient by the end of winter, and deficiency is high even in very sunny countries like India. People who never go out in the midday sun become deficient even on supplementation at 100% of the RDA.

In addition, suntan lotion blocks production. Deficiencies are now much more common in Australia, which had a very successful 'slip slop slap' campaign, though most of the deficient people have dark skin, cover up when outdoors or are confined indoors (e.g. elderly preople or those with a disability or serious illness). This campaign has also taken place in New Zealand. Melanin screens UVB light so dark skin is much less efficient at generating vitamin D. It would therefore be expected that people with darker skin would suffer from deficiencies more frequently, especially if they live at higher latitudes or have an urban lifestyle, and there is much evidence that this is the case. Vitamin D deficiency and osteomalacia are known to be endemic in dark-skinned populations in the UK (particularly those from South Asia).

Vitamin D3 synthesis mechanism

Vitamin D3 is synthesized from 7-dehydrocholesterol, a derivative of cholesterol, which is then photolyzed by ultraviolet light in 6-electron conrotatory electrocyclic reaction. The product is Previtamin D 3.
Previtamin D3 then spontaneously isomerizes to Vitamin D3 in a antarafacial hydride [1,7]Sigmatropic shift.
Vitamin D3 (cholecalciferol) is then hydroxylated in the liver to 25-hydroxycholecalciferol (calcidiol) and stored until it is needed. 25-hydroxycholecalciferol is further hydroxylated in the kidneys to the main biologically active form 1,25-dihydroxycholecalciferol (calcitriol) in a tightly regulated fashion. Calcitriol is represented below right (hydroxilated Carbon 1 is on the lower ring at right, hydroxylated Carbon 25 is at the upper right end).


  1. ^ Coates, M. E. (1968). "Requirements of different species for vitamins". Proceedings of the Nutrition Society. 27 (2): 143–148. PMID 5755261 doi:10.1079/PNS19680039.
  2. ^ "Dietary Supplement Fact Sheet: Vitamin D". National Institutes of Health. Retrieved 2006-06-10.
  3. ^ http://ods.od.nih.gov/factsheets/vitamind.asp
  4. ^ Laurance, Jeremy (28 December 2005). "Revealed: the pill that prevents cancer". The Independent.
  5. ^ Caryl A Nowson and Claire Margerison (2002). "Vitamin D intake and vitamin D status of Australians". The Medical Journal of Australia. 177 (3): 149–152. PMID 12149085.
  6. ^ "RODENTICIDES, source: Journal of Vertrinary Medicine, archives, vol. 27, May, 1998". IPM Of Alaska, Solving Pest Problems Sensibly. Retrieved 2006-07-07. {{cite web}}: Cite has empty unknown parameter: |coauthors= (help)
  7. ^ Adams JS, Lee G (1997). "Gains in bone mineral density with resolution of vitamin D intoxication". Ann Intern Med. 127 (3): 203–206. PMID 9245225.
  8. ^ Rajasree S, Rajpal K, Kartha CC, Sarma PS, Kutty VR, Iyer CS, Girija G (2001). "Serum 25-hydroxyvitamin D3 levels are elevated in South Indian patients with ischemic heart disease". Eur J Epidemiol. 17 (6): 567–71. PMID 11949730.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  9. ^ "Vitamin D 'aids lung cancer ops'". BBC News. 22 April 2005. Retrieved 2006-03-23.
  10. ^ "Vitamin D 'can lower cancer risk'". BBC News. 28 December 2005. Retrieved 2006-03-23.
  11. ^ a b c d e Marshall TG, Marshall, FE (2004). "Sarcoidosis succumbs to antibiotics - implications for autoimmune disease". Autoimmun Rev. 3 (4): 295–300. PMID 15246025.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  12. ^ a b c d e f g Waterhouse JC, Marshall TG, Fenter B, Mangin M, Blaney G. (2006). High levels of active 1,25-dihydroxyvitamin D despite low levels of the 25-hydroxyvitamin D precursor - implications of dysregulated vitamin D for diagnosis and treatment of chronic disease. In VD Stoltz (ed.), Vitamin D: New Research (pp 1-23). New York: Nova Science Publishers.
  13. ^ Mawer EB, Hayes ME, Still PE, Davies M, Lumb GA, Palit J, Holt PJ (1991). "Evidence for nonrenal synthesis of 1,25-dihydroxyvitamin D in patients with inflammatory arthritis". J Bone Miner Res. 6 (7): 733–9. PMID 1950677.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  14. ^ Abreu MT, Kantorovich V, Vasiliauskas EA, Gruntmanis U, Matuk R, Daigle K, Chen S, Zehnder D, Lin Y-C, Yang H, Hewison M, Adams JS (2004). "Measurement of vitamin D levels in inflammatory bowel disease patients reveals a subset of Crohn's disease patients with elevated 1,25-dihydroxyvitamin D and low bone mineral density". Gut. 53 (8): 1129–1136. PMID 15247180.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  15. ^ a b Fauci, A.S. et al. (1998). Harrison’s Principles of Internal Medicine. New York: McGraw Hill.
  16. ^ a b c d Marshall TG. (2006 May). “VDR Nuclear Receptor Competence is the Key to Recovering from Chronic Inflammatory Disease.” Poster session presented at Days of Molecular Medicine Conference, Karolinska Institut, Stockholm, Sweden. Retrieved July 28, 2006 from http://AutoimmunityResearch.org/karolinska-handout.pdf
  17. ^ Kleinberger-Nobel E (1951). "Filterable forms of bacteria". Bacteriol Rev. 15 (2): 77–103. PMID 14847983.
  18. ^ Cantwell AR Jr. (1982). "Histologic observations of variably acid-fast pleomorphic bacteria in systemic sarcoidosis sarcoidosis - a report of 3 cases". Growth. 46 (2): 113–25. PMID 6184266.
  19. ^ Wirostko E, Johnson L, Wirostko W (1989). "Juvenile rheumatoid arthritis inflammatory eye disease. Parasitization of ocular leukocytes by mollicute-like organisms". J Rheumatol. 16 (11): 1446–53. PMID 2600945.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  20. ^ O'Dell JR, Haire CE, Palmer W, Drymalski W, Wees S, Blakely K, Churchill M, Eckhoff PJ, Weaver A, Doud D, Erikson N, Dietz F, Olson R, Maloley P, Klassen LW, Moore GF (1997). "Treatment of early rheumatoid arthritis with minocycline or placebo: results of a randomized, double-blind, placebo-controlled trial". Arthritis Rheum. 40 (5): 842–8. PMID 9153544.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  21. ^ Clark HW, Coker-Vann MR, Bailey JS, Brown TMcP (1988). "Detection of mycoplasmal antigens in immune complexes from rheumatoid arthritis synovial fluids". Ann of Allergy. 60 (5): 394–8. PMID 3369750.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  22. ^ Johnson LA, Wirostko E, Wirostko WJ (1989). "Crohn's disease uveitis. Parasitization of vitreous leukocytes by mollicute-like organisms". Am J Clin Pathol. 91 (3): 259–64. PMID 2923094.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  23. ^ Almenoff PL, Johnson A, Lesser M, Mattman LH (1996). "Growth of acid fast L forms from the blood of patients with sarcoidosis". Thorax. 51 (5): 530–3. PMID 8711683.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  24. ^ Nilsson K, Pahlson C, Lukinius A, Eriksson L, Nilsson L, Lindquist O (2002). "Presence of Rickettsia helvetica in granulomatous tissue from patients with sarcoidosis". J Infect Dis. 185 (8): 1128–38. PMID 11930323.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  25. ^ Mattman, L.H. (2000). Cell Wall Deficient Forms: Stealth Pathogens. Third Edition. Boca Raton, FL: CRC Press.
  26. ^ a b c Marshall TG, Lee RE, Marshall FE (2006). "Common angiotensin receptor blockers may directly modulate the immune system via VDR, PPAR and CCR2b". Theor Biol Med Model. 3 (1): 1. PMID 16403216.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  27. ^ Marshall T.G. (2006) “Molecular genomics offers new insight into the exact mechanism of action of common drugs - ARBs, Statins, and Corticosteroids.” FDA CDER Visiting Professor presentation. FDA Biosciences Library, Accession QH447.M27 2006. Videorecording: http://autoimmunityresearch.org/fda-visiting-professor-7mar06.ram
  28. ^ Evans RM. (2006 June 7). “Nuclear Receptors in Drug-Drug Interactions and Metabolic Disease.” FDA CDER Visiting Professor presentation.
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